ライフサイエンスコーパス: JC virus

1 ous system caused by the reactivation of the JC virus.

2 activation and neurotropic transformation of JC virus.

3 Less than 5% of cases are attributed to the JC virus.

4 brain disease caused by reactivation of the JC virus.

5 ticles (VLPs) derived from the human polyoma JC virus.

6 ntact cells, and cannot distinguish BKV from JC virus.

7 brain cells, termed oligodendrocytes, by the JC virus.

8 ic recognition of a human neurotropic virus, JC virus.

9 nal pathogens, including HHV6, BK virus, and JC virus.

10 from an oligodendrocyte infection caused by JC virus.

11 sus macaque simian virus 40 (SV40) and human JC virus.

12 urine was 400 times higher for BK virus than JC virus.

13 ating myelin-degrading disease caused by the JC virus.

14 der caused by oligodendrocyte destruction by JC virus.

15 cal leukoencephalopathy, associated with the JC virus, a human polyomavirus.

16 d an increase in in vitro CD4+ and CD8+ anti-JC virus activity.

17 The virus was named JC virus after the initials of the patient.

18 us disease in immunocompromised individuals, JC virus and BK virus, encode miRNAs with the same funct

19 nistic brain infection that is caused by the JC virus and is typically fatal unless immune function c

20 However, deeper insight into the JC virus and its pathogenesis and the immune response du

21 lopathy, a rare disease of the CNS caused by JC virus and occurring in immunosuppressed people, is ty

22 drocyte cell line supports both infection by JC virus and robust levels of JCV DNA replication.

23 ecific manner, since T antigen repressed the JC virus and simian virus 40 (SV40) early promoters in g

24 and the other closely related polyomaviruses JC virus and SV40.

25 ls expressed the 5HT2a receptor (5HT2aR) for JC virus and were highly susceptible to infection.

26 with viruses (3 with cytomegalovirus, 2 with JC virus, and 2 with varicella zoster virus) and 3 with

27 infect human beings (simian virus 40 [SV40], JC virus, and BK virus) was associated with non-Hodgkin

28 e, reliable and sensitive PCR testing of the JC virus, and broadened criteria for recognition of PML

29 JC virus antibodies were found in 5 of 13 patients.

30 t demonstrate a 50 to 60% prevalence of anti-JC virus antibodies, a low false-negative rate, and an a

31 Patients who were positive for anti-JC virus antibodies, had taken immunosuppressants before

32 tive or negative status with respect to anti-JC virus antibodies, prior or no prior use of immunosupp

33 actors: positive status with respect to anti-JC virus antibodies, prior use of immunosuppressants, an

34 Positive status with respect to anti-JC virus antibodies, prior use of immunosuppressants, an

35 mong the patients who were negative for anti-JC virus antibodies, with the incidence estimated to be

36 before the diagnosis were positive for anti-JC virus antibodies.

37 lytical false-negative rate of a 2-step anti-JC virus antibody assay.

38 m and plasma samples were collected for anti-JC virus antibody detection using an analytically valida

39 S patients switching from natalizumab due to JC virus antibody positivity at 3 Swedish multiple scler

40 patients who switch from natalizumab due to JC virus antibody positivity.

41 TRATIFY-1 will confirm the stability of anti-JC virus antibody prevalence over time.

42 At baseline (n = 1,096), overall anti-JC virus antibody prevalence was 56.0% (95% confidence i

43 ing age and male gender with increasing anti-JC virus antibody prevalence.

44 Blood samples were available for anti-JC virus antibody testing from 5896 patients with multip

45 Many JC virus antibody-positive relapsing-remitting multiple

46 new tools for risk stratification including JC-virus antibody status, prior immunosuppression, and l

47 yomavirus-specific T cells cross-recognising JC virus antigens.

48 sly demonstrated that T antigen controls the JC virus basal promoter in a glial cell-specific manner,

49 results suggest that T antigen activates the JC virus basal promoter in nonglial cells by interaction

50 These data demonstrate that JC virus binding to human glial cells induces an intrace

51 Advances in the understanding of JC virus biology have shed new light on the pathogenesis

52 opathy, and advances in the understanding of JC virus biology.

53 Human polyomaviruses (JC virus, BK virus and simian virus 40) are causative ag

54 Additionally, the JC virus can also lead to novel neurological disorders s

55 s been demonstrated that the closely related JC virus can enter cells in clathrin-coated vesicles and

56 Recently, we have demonstrated that JC virus can infect cerebellar granule cell neurons and

57 The JC virus capsid is composed of 72 pentamers of the major

58 ypothesis has gained general acceptance that JC virus causes a primary infection in childhood and ent

59 increases CD4+ and CD8+ activity against the JC virus; clinical improvement or stabilization occurred

60 es, but polymerase chain reaction documented JC virus co-infection in one of five cases so tested.

61 rebrospinal fluid revealed 1000 copies/mL of JC virus, confirming the diagnosis of PML.

62 region of the human neurotropic polyomavirus JC virus contains a consensus NF-kappa B site which has

63 It also appeared that archetype JC virus could sporadically be identified in PML patient

64 1 of BK virus with high sequence homology to JC virus counterparts were used to generate polyomavirus

65 Urine was collected for JC virus DNA detection.

66 e clinical presentation and demonstration of JC virus DNA either in the CSF or by histopathology, is

67 own on magnetic resonance imaging regressed; JC virus DNA in plasma, likely originating from the brai

68 JC virus DNA in the CSF and peripheral blood was quantif

69 JC virus DNA may harbor in CD34+ cells in bone marrow th

70 ng oligodendrocytes, which were positive for JC virus DNA on in situ hybridization.

71 JC virus DNA was detectable within cell compartments of

72 up, this increased to 20 patients (71.4%) as JC virus DNA was detected in cerebrospinal fluid of two

73 ient brain, although selection of rearranged JC virus DNA was favored.

74 JC virus DNA was not detected in CSF or peripheral blood

75 right hemispheric and brainstem lesions and JC virus DNA was undetectable in his cerebrospinal fluid

76 at was negative for human polyomavirus 2 (or JC virus) DNA in the cerebrospinal fluid.

77 at was negative for human polyomavirus 2 (or JC virus) DNA in the CSF.

78 The JC virus early promoter directs cell-specific expression

79 a cells but induced strong activation of the JC virus early promoter in nonglial cells.

80 ch as JC virus granule cell neuronopathy and JC virus encephalopathy, and might also cause meningitis

81 The late region of the human neurotropic JC virus encodes a 71 amino acid protein, named Agnoprot

82 The late region of human neurotropic JC virus encodes a small 71-amino-acid agnoprotein that

83 are the requirement with the closely related JC virus for an intact actin cytoskeleton during intrace

84 Isolates of the human polyomavirus JC virus from patients with the frequently fatal demyeli

85 on of the primary tumor may have reactivated JC virus gene expression and led to redevelopment of the

86 Neurotropic JC virus generally harbors reorganized noncoding control

87 lead to novel neurological disorders such as JC virus granule cell neuronopathy and JC virus encephal

88 ge T-antigen (T-Ag) of the human neurotropic JC virus, has been shown to modulate the Wnt-signaling p

89 The human polyomavirus, JC virus, has recently been associated with several huma

90 In contrast, urinary JC virus highly resembled the archetype virus, and urine

91 e with pembrolizumab could reinvigorate anti-JC virus immune activity in patients with PML was unknow

92 TAT1 plays a critical role in the control of JC virus in the central nervous system.

93 encephalopathy patients are now negative for JC virus in the cerebrospinal fluid by polymerase chain

94 confirmed by brain biopsy or by identifying JC virus in the cerebrospinal fluid by polymerase chain

95 cal diagnosis by use of MRI and detection of JC virus in the CSF was established in all but one case.

96 the recent discovery of the presence of the JC virus in the grey matter invite us to reappraise the

97 hs of natalizumab therapy, the prevalence of JC virus in the urine of the 19 patients increased from

98 ew of the possible causes of reactivation of JC virus in this population has illustrated the need to

99 We detected BK and JC viruses in the urine of 35 and 16% of transplant reci

100 ukoencephalopathy caused by John Cunningham (JC) virus in immunocompromised humans.

101 confirming sequences of SV40 (but not BK or JC virus) in his kidney biopsy and urine by polymerase c

102 tem to control the expression of RB2/p130 in JC virus-induced hamster brain tumor cells to study in v

103 revealed typical features of PML as well as JC virus-infected neurons.

104 ndrocyte progenitor cells are susceptible to JC virus infection and indicates that cells poised to re

105 current results enhance our understanding of JC virus infection and PML, and should be taken into acc

106 hese results indicate that susceptibility to JC virus infection occurs at the molecular level and als

107 anagement of IRIS associated with PML due to JC virus infection remains the most challenging, as no a

108 HLA-A*02 persons in response to either BK or JC virus infection.

109 and increases in peripheral CD4+ T cells and JC virus intrathecal antibodies were observed.

110 JC virus is a member of the human polyomavirus family an

111 JC virus is activated to replicate in glial cells of man

112 iological agent of PML, the polyomavirus JC (JC virus), is ubiquitous within the human population.

113 However, T antigen containing the JC virus J domain was functional in these assays, althou

114 e archetype strain of the human polyomavirus JC virus (JCV(Cy)), unlike its neurotropic counterpart (

115 omegalovirus (CMV) was assayed in urine, and JC virus (JCV) and BK virus (BKV) DNAs were assayed in u

116 of the closely related human polyomaviruses JC virus (JCV) and BK virus (BKV) in mesothelioma remain

117 For the human polyomaviruses JC virus (JCV) and BK virus (BKV), the first step to a s

118 of CNS infection, as many viruses, including JC virus (JCV) and HIV, cannot replicate in rodent cells

119 Agnoprotein is a small regulatory protein of JC virus (JCV) and is required for the successful comple

120 detected in all patients, notably including JC virus (JCV) and Torque teno virus (TTV) and interesti

121 undertaken to define the prevalence of anti-JC virus (JCV) antibodies in multiple sclerosis (MS) pat

122 ment is associated with the presence of anti-JC virus (JCV) antibodies.

123 A 55-year-old, JC virus (JCV) antibody-positive patient with multiple s

124 JC virus (JCV) causes progressive multifocal leukoenceph

125 ous system, with the human neurotropic virus JC virus (JCV) causes the fatal demyelinating disease pr

126 otide resolution and relative copy number of JC virus (JCV) clinical standards.

127 determine the clinical utility of measuring JC virus (JCV) DNA in blood or urine of natalizumab-trea

128 The detection and semiquantitation of JC virus (JCV) DNA in cerebrospinal fluid (CSF) is progn

129 JC virus (JCV) DNA in the cerebrospinal fluid (CSF) prov

130 reas transplant patients, BK virus (BKV) and JC virus (JCV) DNAemia were observed most commonly in ki

131 The human neurotropic JC virus (JCV) genome encodes an auxiliary protein calle

132 We sought to determine the prevalence of JC virus (JCV) in bone marrow samples from human immunod

133 JC virus (JCV) infection is a lytic infection of oligode

134 ML), a fatal demyelinating disease caused by JC virus (JCV) infection of oligodendrocytes, may develo

135 natalizumab-treated MS patients is linked to JC virus (JCV) infection.

136 The human polyomavirus JC virus (JCV) infects 70% of the population worldwide.

137 The human polyomavirus JC virus (JCV) infects myelin-producing cells in the cen

138 Infectious entry of JC virus (JCV) into human glial cells occurs by receptor

139 Human polyomavirus JC virus (JCV) is a causative agent of progressive multi

140 JC virus (JCV) is a common human polyomavirus that infec

141 JC virus (JCV) is a human polyomavirus and the causative

142 JC virus (JCV) is a neurotropic polyomavirus infecting g

143 JC virus (JCV) is a polyoma virus that commonly infects

144 JC virus (JCV) is a polyomavirus that ubiquitously infec

145 ts have indicated that the human neurotropic JC virus (JCV) is able to induce cerebellar neoplasms in

146 JC virus (JCV) is latent in the kidneys and lymphoid org

147 cation of the human neurotropic polyomavirus JC virus (JCV) is regulated by cell membrane receptors a

148 The human polyomavirus JC virus (JCV) is the causative agent of the fatal demye

149 The human polyomavirus JC virus (JCV) is the etiologic agent of a fatal central

150 JC virus (JCV) is the etiologic agent of progressive mul

151 The human polyomavirus JC virus (JCV) is the etiologic agent of the fatal demye

152 ur and other laboratories indicated that the JC virus (JCV) late regulatory protein, agnoprotein, pla

153 Infection with JC virus (JCV) may lead to development of demyelinating

154 It has been suggested that JC virus (JCV) might travel to the central nervous syste

155 A comparison of antibody titers to JC virus (JCV) or BK virus (BKV) was made by hemagglutin

156 e diagnosed either using cerebrospinal fluid JC virus (JCV) polymerase chain reaction, brain biopsy,

157 Cell-type-specific transcription of the JC virus (JCV) promoter in glial cells initiates a serie

158 d c-Fos in transcriptional regulation of the JC virus (JCV) promoter in glial cells.

159 Rearrangements of the JC virus (JCV) regulatory region (RR) are consistently f

160 opathy in kidney allograft recipients, while JC virus (JCV) replication occurs in the glial cells of

161 JC virus (JCV) seropositivity is a risk factor for progr

162 To examine the mode of JC virus (JCV) transmission, we collected urine samples

163 JC virus (JCV) viruria is more common than BK virus (BKV

164 de corresponding to the previously described JC virus (JCV) VP1 homolog sequence ILMWEAVTL (JCV VP1p1

165 rt and trafficking of the human polyomavirus JC virus (JCV) with that of simian virus 40 (SV40).

166 disease-causing members (BK virus (BKV) and JC virus (JCV)) identified.

167 for human polyomaviruses: 9 with BKV, 9 with JC virus (JCV), 1 with SV40, and 1 with both JCV and SV4

168 JC virus (JCV), a human neurotropic polyomavirus, demons

169 JC virus (JCV), a human polyomavirus, exhibits oncogenic

170 JC virus (JCV), a human polyomavirus, has been found in

171 JC virus (JCV), a member of the polyomavirus family, cau

172 ML) is a devastating CNS infection caused by JC virus (JCV), a polyomavirus that commonly establishes

173 JC virus (JCV), along with other members of the polyomav

174 Samples were analyzed for BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) by convention

175 Samples were analyzed for BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) using convent

176 d region in the large T antigen gene of BKV, JC virus (JCV), and simian virus 40 (SV40).

177 t three types of polyomavirus infect humans: JC virus (JCV), BK virus (BKV) and Simian Vacuolating vi

178 association of 4 human polyomaviruses (HPyV)-JC virus (JCV), BK virus (BKV), human polyomavirus 6 (HP

179 tifocal leukoencephalopathy (PML), caused by JC virus (JCV), can occur in patients receiving natalizu

180 The human polyomavirus, JC virus (JCV), encodes two regulatory proteins at the e

181 astating demyelinating disease caused by the JC virus (JCV), for which no therapeutics are approved.

182 tional regulation of the human polyomavirus, JC virus (JCV), genome.

183 ection of the ubiquitous human polyomavirus, JC virus (JCV), in samples derived from several types of

184 iruses, including Simian Virus 40 (SV40) and JC virus (JCV), is a multifunctional phosphoprotein that

185 on of glial cells by the human polyomavirus, JC virus (JCV), leads to a rapidly progressing and unifo

186 JC virus (JCV), the causative agent of progressive multi

187 JC virus (JCV), the causative agent of the fatal human d

188 pathogen-specific primers to detect DNA from JC virus (JCV), varicella zoster virus (VZV), cytomegalo

189 n paid to human polyomaviruses, particularly JC virus (JCV), which infects greater than 80% of the hu

190 ncomitant presence of the human papovavirus, JC virus (JCV), which is the etiologic agent of the suba

191 f the central nervous system (CNS) caused by JC virus (JCV), which occurs in immunocompromised indivi

192 to 80% of humans express serum antibodies to JC virus (JCV), yet considerably fewer people develop PM

193 is the most common clinical presentation of JC virus (JCV)-associated central nervous system (CNS) d

194 linked immunosorbent assay (ELISA) to detect JC virus (JCV)-specific antibodies in multiple sclerosis

195 JC virus (JCV)-specific CD8+ cytotoxic T lymphocytes (CT

196 JC virus (JCV)-specific cytotoxic T lymphocytes (CTL) in

197 tion of glial cells by the human neurotropic JC virus (JCV).

198 endrocytes by the opportunistic polyomavirus JC virus (JCV).

199 ised individuals are infected with the human JC virus (JCV).

200 an genotypes (Types 2 and 7) and subtypes of JC virus (JCV).

201 ation of the human neurotropic polyomavirus, JC virus (JCV).

202 eactivation of BK virus (BKV) or more rarely JC virus (JCV).

203 s and replication of some viruses, including JC virus (JCV).

204 an immunodeficiency virus type I (HIV-1) and JC virus (JCV).

205 ral nervous system, by the human neurotropic JC virus (JCV).

206 omoters of the ubiquitous human polyomavirus JC virus (JCV).

207 s of human polyomaviruses BK virus (BKV) and JC virus (JCV).

208 gered by infection with the human gliotropic JC virus (JCV).

209 for sustaining the productive replication of JC virus (JCV).

210 al disease caused by the reactivation of the JC virus (JCV).

211 demyelinating disease of the brain caused by JC virus (JCV).

212 e DNA recombination between polyomavirus JC (JC virus [JCV]) and Epstein-Barr virus (EBV) at sequence

213 V-6B, herpes simplex virus 1 [HSV-1], HSV-2, JC virus [JCV], and varicella-zoster virus [VZV]).

214 n between large T antigen and Rb proteins in JC virus-mediated oncogenesis.

215 n immunosuppressed macaques, which parallels JC virus-neuronal infection in immunosuppressed patients

216 may be an important aspect of both SV40 and JC virus neuropathogenesis in their respective hosts.

217 Subclinical reactivation of JC virus occurs frequently in natalizumab-treated patien

218 due to BK virus, but rare cases result from JC virus reactivation.

219 chain-reaction assays in blood and urine for JC virus reactivation; BK virus, a JC virus-related poly

220 In addition, we have determined that JC virus readily infects G144 cells.

221 JC virus regulatory-region sequences in blood samples an

222 zyme-linked immunosorbent assay and analyzed JC virus regulatory-region sequences.

223 urine for JC virus reactivation; BK virus, a JC virus-related polyomavirus, was used as a control.

224 nd its recurrence for their association with JC virus revealed that, while the viral genome is presen

225 different rearrangements were present in the JC virus sequences present in the WHO standard across mu

226 uppressive agents (n = 8), and reported anti-JC virus seropositivity (n = 13).

227 strong cellular immune response mediated by JC virus-specific CD8 cytotoxic T lymphocytes, which are

228 The JC virus-specific cellular immune response dropped signi

229 g is associated with a transient drop in the JC virus-specific cellular immune response.

230 We determined JC virus-specific T-cell responses by means of an enzyme

231 JC virus susceptibility correlated with significantly hi

232 s were not cross-reactive on the human BK or JC virus T ags.

233 n, 18q LOH was independently associated with JC virus T antigen (odds ratio [OR] = 1.93; P = .0077),

234 The IRS-1 domain responsible for a direct JC virus T-antigen binding was localized within the N-te

235 nt of IRS-1 inhibited growth and survival of JC virus T-antigen-transformed cells in anchorage-indepe

236 pe, LINE-1 methylation, and John Cunningham (JC) virus T antigen.

237 is an opportunistic infection caused by the JC virus that has no proven effective treatment.

238 endrocyte progenitor cells to infection with JC virus, the causative agent of progressive multifocal

239 Most adults who are infected with the JC virus, the etiologic agent in PML, do not have sympto

240 protein activates the major late promoter of JC virus through a Tat-responsive DNA element, termed up

241 ogy, representing the immune response to the JC virus to a variable extend.

242 Simian virus 40 and JC virus, two closely related members of the polyomaviru

243 d large T antigen expression by BK virus and JC virus, two important, pathogenic human polyomaviruses

244 for both murine polyomavirus and SV40, while JC virus uses serotonin receptors.

245 After 18 months of treatment, JC virus was detectable in 3 of 15 available plasma samp

246 ncephalopathy or evidence of reactivation of JC virus were identified.

247 of SV40 VLPs but not by VLPs for BK virus or JC virus, which are related human polyomaviruses) was in

248 isease that results from reactivation of the JC virus, which generally occurs in immunosuppressed hos

249 rtunistic infection of the CNS caused by the JC virus, which infects white and grey matter cells and

250 tter of the brain caused by the polyomavirus JC virus, which typically occurs only in immunocompromis